CAJ | 학술논문

目的：探讨小胶质细胞吞噬α‐突触核蛋白的分子机制。方法构建α‐Syn寡聚体诱导BV‐2细胞活化模型，免疫荧光检测BV‐2细胞内α‐Syn阳性包涵体的数量。Western blot检测BV‐2细胞LRRK2蛋白的表达。Pull down检测BV‐2细胞Rac1、Cdc42、RhoA的活性。结果与对照组相比，α‐Syn寡聚体诱导BV‐2细胞内α‐Syn阳性包涵体数量增加，LRRK2蛋白表达增加及Rac1、Cdc42、RhoA活性增加。结论小胶质细胞对α‐突触核蛋白的吞噬与LRRK2活化Rho GTPases信号通路相关。
목적：탐토소효질세포탄서α‐돌촉핵단백적분자궤제。방법구건α‐Syn과취체유도BV‐2세포활화모형，면역형광검측BV‐2세포내α‐Syn양성포함체적수량。Western blot검측BV‐2세포LRRK2단백적표체。Pull down검측BV‐2세포Rac1、Cdc42、RhoA적활성。결과여대조조상비，α‐Syn과취체유도BV‐2세포내α‐Syn양성포함체수량증가，LRRK2단백표체증가급Rac1、Cdc42、RhoA활성증가。결론소효질세포대α‐돌촉핵단백적탄서여LRRK2활화Rho GTPases신호통로상관。
Objective To investigate the mechanism of microglial phagocytosis of α‐synuclein.Methods BV‐2 cells activa‐tion model induced by α‐synuclein oligomers was established. Immunofluorescence stain was performed to detect α‐synuclein‐positive inclusions in BV‐2 cells. Western blot was performed to detect LRRK2 expression in BV‐2 cells. Pull down was per‐formed to detect Rho GTPases signaling pathway activation in BV‐2 cells.Results Compared with the control group ,α‐synucle‐in‐positive inclusions ,LRRK2 expression and Rho GTPases signaling pathway activity in BV‐2 cells significantly increased in theα‐synuclein group.Conclusion The Rho GTPases signaling pathway activation induced by LRRK2 associate closely with mi‐croglial phagocytosis of α‐synuclein.